1. Patients launch $1.27 million crowdfunding campaign for ME/CFS gut microbiome study.
    Check out the website, Facebook and Twitter. Join in donate and spread the word!
Nitric oxide and its possible implication in ME/CFS (Part 2 of 2)
Andrew Gladman explores the current and historic hypotheses relating to nitric oxide problems in ME/CFS. This second article in a 2-Part series puts nitric oxide under the microscope and explores what it is, what it does and why it is so frequently discussed in the world of ME/CFS....
Discuss the article on the Forums.

Cross Party Group on ME

Discussion in 'General ME/CFS News' started by Yogi, Oct 9, 2012.

  1. heapsreal

    heapsreal iherb 10% discount code OPA989,

    Messages:
    7,149
    Likes:
    4,403
    australia (brisbane)
    I have read the first and the last page and really think the arguement about me and cfs should be left alone until there are better biomarkers which hopefully arent too far away. I know finding a biomarker is hard when there is a mixed bag of patients but i think the vast majority of patients with either diagnosis have the same condition just in varying severity and symptoms.

    The nk bright cell dysfunction to my knowledge is mainly found in cfs/me, rheumatoid arthritis and MS patients??? i think?? Last i heard PHANU are looking into how to seperate these 3 conditions through further nk function testing.

    If they find a specific nk dysfunction only common to cfs/me, then i hope they get rid of both names as both names have been muddied beyond repair that many doctors will never recognise as then they would be admitting they were wrong. NK neuro-immune dysfunction for example or something very descriptive of the illness. I think ME is a fine description but the term is now damaged and past its used by date.

    cheers!!
  2. user9876

    user9876 Senior Member

    Messages:
    707
    Likes:
    1,630
    There is a big difference between deciding on criteria for a cohort for research and a more general diagnostic one. With research we should push for either very large sets of patients or well defined cohorts (even if they only include a subset of ME patients).

    I agree in more general terms that we should leave the separation of the names ME and CFS for the moment. I'm not convinced that they are separate although I think there are people who are misdiagnosed with a CFS/ME label when they have something else wrong.
    Adamskitutu likes this.
  3. Ember

    Ember Senior Member

    Messages:
    1,728
    Likes:
    1,779
    Myalgic encephalomyelitis: International Consensus Criteria

    http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2796.2011.02428.x/full
  4. Ember

    Ember Senior Member

    Messages:
    1,728
    Likes:
    1,779
    “The New International Consensus Criteria for M.E. - content and context” by Bruce M. Carruthers:
    http://investinme.org/Documents/Journals/Journal of IiME Vol 6 Issue 1 Screen.pdf
    Bob likes this.
  5. Ember

    Ember Senior Member

    Messages:
    1,728
    Likes:
    1,779
    Myalgic encephalomyelitis - Adult & Pediatric: International Consensus Primer for Medical Practitioners
    http://hetalternatief.org/ICC%20primer%202012.pdf
  6. Valentijn

    Valentijn Activity Level: 3

    Messages:
    6,041
    Likes:
    8,403
    Amersfoort, Netherlands
    I'm not Alex, but for starters muscle twitches sound a lot more like a sign than a symptom. Unless it's possible for us to fake an isolated muscle visibly jumping around for a while?

    I suppose abnormal neurotransmitter levels could be considered a sign of neurological dysfunction as well, even if the levels do not originate as the result of a neurological problem.

    And on a bad day, I develop a severely ataxic gait after doing "too much", which can vary between having walked for half an hour or trying to walk at all. This seems to be related to orthostatic intolerance in my case, since the problem has largely disappeared while taking OI meds.

    Oh, and I suppose some forms of OI are themselves signs of neurological dysfunction, easily measurable by such cutting-edge technology as a blood pressure monitor and a heart rate monitor.

    There's no single specific neurological sign saying "THIS IS ME/CFS AND ONLY ME/CFS", but there are plenty of signs - unless you're a neurologist that believes ME/CFS is entirely psychological and any neurological signs necessarily mean you have a "real" disease, not ME/CFS.
  7. user9876

    user9876 Senior Member

    Messages:
    707
    Likes:
    1,630
    Thats the whole point isn't it. It makes sense to remove people with other diseases (that cause fatigue etc) from a ME/CFS diagnosis. What you are then left with is a set of people who have fatigue along with a range of other symptoms that are currently unexplained. They may all have the same cause or they may not. As a researcher or doctor it may be useful to further subdivide according to the research hypothesis being explored or because people with particular symptoms respond in someway to a given drug. However until we have more of an idea of bio markers and mechanism its making further generalised divisions seems quite arbitary.
  8. alex3619

    alex3619 Senior Member

    Messages:
    7,018
    Likes:
    10,794
    Logan, Queensland, Australia
    Replying to Firestormms post 300 on neurological signs.

    Anything that can be confirmed by a test is a sign, not a symptom. So gait ataxia is a sign. Slowed cognitive processing is a sign. Poor executive brain function, dysautonomia of various kinds, central sleep apnoea, altered sleep patterns (investigated in a sleep lab), peripheral neuropathy ... all neurological signs. Furthermore many of us, though based on a tiny autopsy sample size so far, probably have lesions in the dorsal root ganglia. These same kinds of lesions developed when monkeys were injected with plasma from ME patients from the 1949 ME atypical polio epidemic. I suspect obstructive sleep apnoea is also neurological, though this is not absolutely clear.

    None of these are mandatory for ME. Many of these do however fulfil parts of an ME diagnosis. The problem is, I suspect, many neurologists have bought the idea that CFS and ME cohorts are identical patient cohorts, and CFS in the UK does not require neurological signs.

    The other problem is that nearly all of these require expensive and time consuming tests. They cannot be done routinely by a neurologist in a clinic. Dorsal root ganglia lesions are also only visible on autopsy .. not very useful clinically.

    Bye, Alex
  9. barbc56

    barbc56 Senior Member

    Messages:
    1,354
    Likes:
    718
    Hi Alex, I have obstructive sleep apnea and it is not neurological but it's structural issue.For years my dentist would remark about how hard it is to work on my teeth because of the structure of my mouth. As you get relatively older usually between 40-50, the muscles in your mouth and throat become more lax and if you have a certain structure your tongue goes back and blocks the airway.Low and behold I went for a sleep study and found out I do indeed have sleep apnea. I knew I snored but had no idea I would stop breathing for at least ten seconds 51 times per hour during deep sleep, which interrups your sleep. Anything over 5 times per hour needs to be treated.

    Even though the CPAP, which is nothing like the CPAP's of old, has corrected this I have not seen that much of a difference in my pain levels and exhaustion As my neurologist says I still have this DD. However, if not treated, OSA has a big impact on your health, especially your heart, blood pressure and can even cause sudden death.

    Central apnea is caused by untreated OSA as the repeated apneas can rewire the brain.

    I have always said anyone with our illness needs to get at least an overnight sleep test. Not just for OSA but a myriad of other conditions and as you know for most of us sleep is really related to this illness. I still have two other sleep disorders.

    Barb C.

    ETA I just want to mention that many people think you have to be overweight to have OSA but a majority are not. You can also have OSA without snoring but that is a rarer The population who are at most risk to develope OSA are football players as many have a thick neck circumfrence. I am speaking of american foot ball.
    Bob and PhoenixDown like this.
  10. alex3619

    alex3619 Senior Member

    Messages:
    7,018
    Likes:
    10,794
    Logan, Queensland, Australia
    HI barbc56, half of all CFS (not ME diagnosed) patients with obstructive sleep apnoea do not respond to CPAP, something most sleep specialists are unaware of. I am one of them. The second issue is I used to talk with a researcher who identified a biochemical neurological trigger for an apnoea event - acetylcholine in the brain stem. I do not know if this was published however. While structural issues can predispose to an apnoea event, including excess weight, the event itself probably has a neurological basis in at least a subset.

    So far as I am aware most with central sleep apnoea show no signs of obstructive sleep apnoea.

    Bye, Alex
  11. barbc56

    barbc56 Senior Member

    Messages:
    1,354
    Likes:
    718
    Sorry to hear you don't respond to CPAP. Do you mean you don't get any symptom relief with treatment or that your apnea has not improved.?

    Only about 5% of patients diagnosed with sleep apnea have central-sleep-apnea. There are several types of central-sleep-apnea conditions and many of these are caused by underlying medical disorders whereas OSA is purely structural. Idiopathic central-sleep-apnea is the rarest form of CSA.

    Central-sleep-apnea is strongly associated with structural sleep-apnea and may be causal as well. If you have both you have mixed sleep apnea.
    http://emedicine.medscape.com/article/304967-overview
    http://www.kevinmd.com/blog/2011/06/differences-obstructive-central-sleep-apnea.html

    It's quite rare that someone would see no improvement as far as apnea events with CPAP. This makes me wonder about the accuracy that half of CFS patients don't respond to CPAP, as patients with neurological as well as other medical conditions will see some improvement in apnea events even if it is only a relative number of reductions. I see my sleep neurologist next month and will also ask for his imput.

    I've only seen a slight improvement in my symptoms since starting the CPAP. even though my apnea events have decreased pretty much to normal. However, this should help decrease further health problems down the road. Hopefully.
    Barb C.:>)

    ETA Have you seen your sleep specialist recently?
  12. alex3619

    alex3619 Senior Member

    Messages:
    7,018
    Likes:
    10,794
    Logan, Queensland, Australia
    There was a clinical trial of CPAP on CFS patients with obstructive apnoea some years ago. They were expecting it would be successful. They found half still had unrelieved apnoea even though they were on CPAP. If it were structural they should have responded. In addition if you inject acetylcholine into mouse brain stems, mice get it too, if I recall the research I was referring to earlier correctly. The researcher was at University of Qld, around 2002. I no longer recall his name. We had quite a long discussion about CFS, as Vance Spence had just published (2000) about an acetylcholine link to vascular problems in CFS.

    Similarly many of us have rhinitis, but only half respond to steroidal treatment. Things are happening that do not fit the standard medical model. What they are exactly has never been properly investigated.

    Bye, Alex
  13. barbc56

    barbc56 Senior Member

    Messages:
    1,354
    Likes:
    718
    I would be very interested in actually reading this study.

    It would seem to me if the patients were diagnosed with obstructive sleep apnea which means theres a structural problem, you would have to see some difference just from the physics of how the CPAP works. It would mean the obstruction would have to be very severe. I could see this possibly happening in central apnea. As I said this is about structure and the physics which should make some kind of difference. Unless you are talking about central apnea.

    This could all very well be true but it just doesn't make sense to me knowing what I know about sleep apnea, but I am not a doctor. Maybe if I had some hard data in front of me it would make more sense.

    Just in the last three years great strides have been made not only with the technology but also the understanding of what is happening in OSA or CSA.

    But we are getting off topic again and if you wish to discuss it further feel free to start a new thread.

    Barb C.:>)
  14. alex3619

    alex3619 Senior Member

    Messages:
    7,018
    Likes:
    10,794
    Logan, Queensland, Australia
  15. barbc56

    barbc56 Senior Member

    Messages:
    1,354
    Likes:
    718
    Thanks, Alex. I havn't had a chance to read this in detail but it looks interesting.
    Barb C.:>)
  16. Firestormm

    Firestormm Guest

    Messages:
    5,824
    Likes:
    5,965
    Cornwall England
    Here you go Ember. A lady after your own heart and Scottish to boot:
    Collapse of Scottish Cross Party Group on ME: http://www.velo-gubbed-legs.blogspot.co.uk/2012/10/collapse-of-scottish-cross-party-group.html

    I have a lot of respect for Nasim incidentally although we have 'crossed swords' once or twice in the past.

    I think previously in this thread Mark mentioned that 'many' of the people with this condition he speaks to regard themselves as having 'ME' and that 'ME' is the more recognised/regarded term - and that's half the problem right there.

    We now seem to be at a stage where anyone who is bed-bound and/or in the 'severe' category (variously defined) is seen as having 'ME'. That even now with the lauded ICC ME patients can 'simply' state 'I have that! I have neurological ME and you lot ain't doing enough for me with that psycho-mumbo-jumbo'.

    As Heaps said above - I believe we cannot simply draw a line based on subjective symptomology and unproven unaccepted test results.

    For a patient the great hope is that a correct diagnosis will lead to better treatment, treatment that will turn around or lessen their suffering.

    Slapping a diagnosis of 'ME' onto someone in the way that is being touted does not achieve that. You will still be 'treated' the same by the NHS.

    Some of us might 'feel' better. Might 'feel' more deserving. Hell it 'might' impact on any benefit or insurance claims - though I don't understand why when 'CFS/ME' is accepted as largely neurological anyway; but I think we are kidding ourselves here.

    The fight to maintain independence - to maintain the label (for that is all it ever was) - of 'ME' was lost way back in the mists of time and buggar all has changed to enable a better prosecution.

    The current state of play is that if you meet the NICE Guideline (presuming that a doctor correctly adheres to it), then as a patient you can refer to yourself as having CFS or ME's.

    It is hardly a satisfactory position, but it is what we have now. I don't know where Scotland are going now that the CPG has collapsed, but I do know that the NICE Guideline has not been fully implemented anywhere in the UK to it's fullest extent.

    Personally, I want now to see all PCT's and GP Commissioners 'lobbied' by Government and Patient organisations to implement to Guideline across the board. Why?

    Because nobody to date have ever carried out the research embedded in the Guideline that would allow for example, data to be gathered on the ground into such things as patient numbers and the effectiveness of current treatment options, to discover how many patients might have another condition e.g. a misdiagnosis etc. etc. etc..

    Until such time as we have better evidence for the effectiveness or lack of of those treatments you all generally abhor from 'real-life' patients in our communities - we cannot possibly lobby for change.

    If we can show that people are not being offered the full NICE Guideline - if we can show that local PCT's are not providing the funding - if we can show that those patients who do agree to try the three interventions (over and above any prescribed medications) we are barking in the dark.

    Not to mention that I still regard Encephalomyelitis as completely the wrong bloody term, and that whilst we all enter this diagnosis with various triggers we are all assumed to have the same damn thing.

    Why is it that someone who gets my diagnosis due to a chemical exposure is assumed to be not only affected in the same way as I am (with a viral trigger) but is offered the same treatment options in terms of management?

    I don't get this and I never really have. Not enough has been done in my view to consider sub-categorising based on established triggers though I realise that (I think) Switzerland are looking at this from one angle at least.

    I think the labelling is the wrong thing to continue lobbying about. It is a dead duck. You ain't gonna see any separation of the terms used even with startling research. Our condition will come to be increasingly regarded as a spectrum based on severity.

    Sorry. Bit garbled. Picked up a damn cold from my niece. Anyway, am back you poor sods :)

    Fire
    heapsreal likes this.
  17. Firestormm

    Firestormm Guest

    Messages:
    5,824
    Likes:
    5,965
    Cornwall England
    Hi chaps,

    I think you are both wrong about this and here's why. A doctor has to observe a symptom and recognise it as a neurological sign. It has to be obvious and also something that is indicative of a likely problem outside of what might already have been diagnosed.

    An example of personal nature. Seizures. I had them. Still get them. These were observed. There were diagnosed as being something outside of my existing diagnosis (ME). I received (what I recall as being) an EEG. As a result I had an epilsepsy diagnosis attached. I receive specific pills for that. It has helped better manage the frequency and extent of these episodes.

    My muscle twitching, was not considered something worth further testing. However, it was regarded as a symptom of my ME. I was prescribed Baclofen. It has helped. Not cure. But helped as well as helping relax my muscles generally - aiding what little sleep and relaxation I can achieve.

    Here's another. Drunken wobbling about the place. This was observed clearly. At work. Was even accused of being drunk. The bastards. Accompanied by Nausea. Constant. Now this one took some time to get treated but again no specific tests were made. Eventually I saw a specialist in ME and was prescribed Betahistine Dihydrochloride. It not only fixed (largley) the nausea (thank the Gods and praise be!) but it has helped stablise what was previously always considered some labyrinthine dysfunction and indeed still might be.

    How about encephalitis? Now I had that diagnosed: 'viral encephalitis'. Way back when I also had a diagnosis (or before I can't remember) of PVFS after a failed recovery from the Parvo-virus that kicked all this off for me). How was that diagnosed? I honestly do not know. There were not obvious or specific symptoms, nor were there SIGNS that I could point to. But two doctors came to the same conclusion. What was the result? Nada. There was no specific treatment recommended.

    Now, take the trembling that is associated with Parkinsons. Right? Deemed to be a neurological SIGN. For a doctor who is listening to what the patient is describing (completely i.e. holistically/whatever), and observing, (because it's far more than simply having a trembling arm - e.g. one might enquire of the patient: 'Does the trembling stop when you grip a glass of water?') he might conclude - right this looks like it could be Parkinsons' Better run some further tests and refer to neurologist.

    Same, for Multiple Sclerosis. Signs may well be observed represented as symptoms from the patient point of view or anomalies, strange behaviour, inability to control limbs, weakness, whatever. But the doctor has to associate them with what might be a SIGN of something deeper and refer accordingly.

    Sometimes it can take a while.... Sometimes you get shit doctors.... Sometimes as a patient you don't do enough of a good job in explaining how changes are affecting you... Lots of reasons SIGNS might be missed or confused with other things, but 'ME' is not recognised as having any CLEAR NEUROLOGICAL SIGNS and more importantly perhaps - a diagnosis of 'ME' is able to be applied without further investigation and/or testing.

    Why should e.g. a neurologist become involved and/or carry out further testing to confirm a diagnosis of something that can be diagnosed with the current NICE Guideline?

    Because until such time as we are able to research the effectiveness of the NICE Guideline - or even compare the CCC with ICCME on the ground in real life - then what's the point for either the improved patient outcome or in terms of additional cost to the NHS?

    What I mean is - anyone wishing to claim that 'ME' is somehow different to 'CFS/Whatever' is going about it the wrong way in my opine.

    You need to be able to demonstrate that patients with 'ME' will have an improved outcome if they were so diagnosed and that the extra expense can be justified.

    Flinging tests at the establishment who don't recognise them ain't gonna cut the mustard. They will and are able to say - so what? In what way will patients benefit? In what way can we justify the added expense?

    Well that's a couple of things that say I think. But mainly you'll need to better fight for on the ground research data reporting back to a central source that undermines the existing patient outcomes from the three therapies generally recommended: activity management (Severe), CBT and GET (Moderate and Mild).

    Anecdotal patient reports - the MEA Survey even whilst good - doesn't really bring home any message being shouted from the rooftops by the loudest few I am afraid.

    p.s. added edit about encephalitis above
    Bob likes this.
  18. alex3619

    alex3619 Senior Member

    Messages:
    7,018
    Likes:
    10,794
    Logan, Queensland, Australia
    Hi Firestormm, its not enough that a doctor can observe a symptom, they must also recognize its importance for it to be a recognized sign - which is more or less what you stated, but its about mechanisms. A sign has to be associated with known mechanisms so far as I can see. In the case of muscle twitching, yes its a sign - probably a neurological sign, but it doesn't have to be. It could be metabolic. In the case of stumbling about as though drunk, thats an observable symptom. It could be anything ... including play acting. Thats how many docs would view it unless they made further tests.

    Reflex tests (usually normal) and Rhomberg tests (may not be normal) can be done easily in a clinic, as can pupilary dilation testing (which can show light sensitivity). Blood pressure crashes can also be observed if they just bother to do the testing right. Its just that the most useful tests for ME cannot be done in a clinic.

    Maybe one of the doctors on this forum could comment?

    Regarding non-acceptance of tests, I agree, but that wasn't the question I was addressing. In the UK so many tests are ignored even though they WOULD assist the patient. To claim otherwise on many tests is simply false: its spin for bureaucratic purposes. Lets save money at the patient's expense.

    One of the main outcomes of this is to avoid having to recognize disability and therefore grant state benefits. Doctors have an obligation to effectively diagnose, not just treat. In addition with a nearly 50% misdiagnosis rate in the UK I would think that alone was grounds for more testing. Tilt table testing and mitochondrial function testing are two tests that should be used. Tilt table testing has been extensively researched and may indicate autonomic dysfunction. Mitochondrial function testing is new and not really replicated in published science, but neurons are very vulnerable to low energy production.

    Such tests will usually be negative for Oxford "CFS" patients, so its a justifiable (but misleading) claim to say its not cost effective. For ME patients however such tests routinely show major problems, so if ME were accepted these costs would be justified.

    The 50% misdiagnosis rate is compounded by the non-attendance of the very severe patients. Many "CFS" doctors do not even see severe patients, and are generally unaware of their existence. This biases their viewpoints.

    Doctors not recognizing signs does not mean they are not there. It only means the doctor failed to find them, or is unaware of the science. How are spinal lesions, brain lesions, or heart lesions not signs? They are objectively verifiable pathophysiology that can underlie patient symptoms You can argue about the significance, or the justification for testing, but those are different questions.

    One of the most clinically useful and frequently associated signs is not neurological - its post exertional energy crash following exercise. This can be verified by the Stevens protocol, and is objective. I think most Oxford "CFS" patients would not show problems here, though that has yet to be confirmed scientifically, but most ME patients would. This test is however expensive and time consuming, and cannot be used on very severe patients (and probably many severe patients). The crash is a symptom. It becomes a sign when it can be objectively verified.

    Similarly a substantive reduction in heart ejection fraction is closely associated with ME. I doubt it would be associated with Oxford "CFS".

    I wonder how much of this is pointless semantic argument though? I doubt much of this matters to the NHS and NICE. They manage medicine, they don't treat it as science.

    The major reason for the use of ME definitions though is not clinical, its research based. The "Oxford" definition is the worst possible choice for a research definition.

    On a separate issue I don't think ME as a distinct disease entity has been proven. Further, I think the diagnosis will disappear once the science has objective and accurate diagnostic biomarkers and we better understand the pathophysiology. Any label in use is a temporary one.

    Bye, Alex
    Valentijn likes this.
  19. Mark

    Mark Acting CEO

    Messages:
    4,513
    Likes:
    1,929
    Sofa, UK
    I'm not sure exactly what I said earlier, but I don't see why it is a problem that most people in the UK recognise the term ME. To clarify what I was (presumably) referring to earlier: a couple of people I know were diagnosed with "ME" before the term "CFS" was invented, every patient I have spoken to in the UK personally calls it "ME", and most significantly of all I have never met a member of the general (non-patient) public who has even heard of the term "CFS". Everybody I have ever spoken to just calls it "ME", and every patient charity in the UK has "ME" in their name. As far as I can see, it is only the Wessely school researchers who have imported the term "CFS" in their research, and are now trying to shift the balance from "ME/CFS" to "CFS/ME" and (eventually) just "CFS". The fact that they are so concerned about the name change, and many of them seem more than happy to shorten this to simply "chronic fatigue", seems to me the most telling evidence that the name does, in fact, matter.

    "ME" is the historical term in the UK to describe the disease, whereas the conception and adoption of the term "CFS" is based on the belief that the disease called ME does not really exist (eg: "Is this not the Royal Free Disease and therefore questionable as a disease entity?") and that those who suffer from it merely have a syndrome of "chronic fatigue" and should be studied as part of the wider group of all patients with unexplained chronic fatigue. I use "ME/CFS" purely as a compromise to communicate with patients in the US, many of whom only know it as "CFS". In the UK, there would be no need for that compromise and I would definitely advocate the use of the term "ME", because even if it is not a perfect characterisation of the disease, it's a better characterisation than "CFS", it's the term that is most widely recognised, and it's the name used by all the charities. Until there is a better understanding of the causes and pathophysiology, it's at least as good a name as any other and I think we should stick with that.

    In the UK context, the term "ME" was coined after the Royal Free outbreak and it was used then, and has been used since, to describe the illness/disease we understand when we consider criteria like the CCC and the ICC. After the Lake Tahoe outbreak, the term "CFS" was coined by people who believed that the illness of people in the outbreak was psychosomatic, and the intention and the result of that new terminology has been to study people with our illness under the umbrella of "all people with unexplained chronic fatigue". This could conceivably be justified by arguing that the details of the subsets of this wider group need to be studied in depth before discrete clinical entities like "ME" can be considered proven, and I think that is the essence of your argument, Firestormm. However, the evidence that the researchers coining and using the term "CFS" are not interested in doing that subsetting is overwhelming. Their studies do not aim to stratify or subset at all; instead, they broaden the definition to include more and more patients with chronic fatigue and then conduct studies that treat those patients as if they were a homogeneous group.They then reach conclusions and apply them to everyone with this diagnosis. This strategy can be and is used to "disprove" or cast doubt upon any findings of other researchers regarding "ME". If another group finds that 66% of people with CCC ME are completely cured by Drug X, the Oxford criteria researchers can show you that only 10% of their group are helped by it and use that as an argument to muddy the waters and slow progress, and that is how scientific progress on studying ME/CFS continues to be blocked.

    Thus the most crucial points we should remember in all of this, are that broadening the definition of the waste-basket into which we are all dumped by people who do not believe we are really physically ill does not serve our interests, that in practice no attempt is being made to explore subsets of this ever-expanding definition, and that the name "chronic fatigue syndrome", by its very nature, serves to reinforce this enormously unhelpful and damaging strategy for the treatment of our illnesses. Precisely how we might best adapt strategy and respond to that is another matter - I do not think it is necessarily the best strategic option to continue to try to fight against that tide and we might perhaps do better by (for example) campaigning for studies to explore subsets of what they call "CFS" - but I do think it's important in the context of an argument such as the subject of this thread to understand the history of how and why the term "CFS" was coined, by whom, and how it has in practice made effective research conclusions impossible and changed the management of our illness for the worse for the last 25 years.

    In the end, the bottom line for me is a simple, logical point. If it is accepted that the condition as defined by Oxford is a highly heterogeneous group (and Wessely and others have asserted this, as an argument as to why any research that finds a single cause must be wrong), then it logically follows that the appropriate first step towards meaningful research is to identify meaningful subsets within that broad definition. The fact that this has not been done and is not being done tells us all we need to know about the reasons for the lack of progress in the recognised understanding of our illnesses, and regardless of the arguments over the ME definition and the best name to use, that inconsistency in the approach of the Wessely School deserves to be highlighted. If they claim it is a heterogeneous definition, they should not also be asserting that conclusions from their research can and should be applied to the entire group without any attempt at subsetting. In that context, it's entirely understandable that patients who once had a clear diagnosis with a massively more restrictive criteria, which has been subsumed into a wider definition that prevents any medical progress, are arguing as they are for the retention and definition of the term "ME".
    currer, Bob and Valentijn like this.
  20. heapsreal

    heapsreal iherb 10% discount code OPA989,

    Messages:
    7,149
    Likes:
    4,403
    australia (brisbane)
    ME seems to be a term used in the UK and CFS is a term used in the USA. Australia use to use the term ME but we seem to follow the Americans with most things so now the term cfs is used more. Most of the research in the last 20 years has been on the cfs term but its still relevant to ME, there interchangable names depending on where one lives.

See more popular forum discussions.

Share This Page